ArticlePloS one2010
The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.
- Pooled it
- Regulation of Intestinal Inflammation by Dietary Fats.Frontiers in immunology · 2020Pooled it
- Regulating arachidonic acid metabolism: a novel strategy to prevent colorectal inflammatory cancer transformation.Journal of Cancer · 2025Review
- Mutation of the cyclooxygenase 2 gene promoter and anastomotic leakage in colorectal cancer patients: retrospective cohort study.BJS open · 2024Article
- Apolipoprotein A-I mimetics mitigate intestinal inflammation in COX2-dependent inflammatory bowel disease model.The Journal of clinical investigation · 2019Article
- Genetic Variations in Inflammatory Response Genes and Their Association with the Risk of Prostate Cancer.BioMed research international · 2015Article
- Pharmacogenetics of analgesic drugs.British journal of pain · 2013Article
- Cyclooxygenase-2 genetic polymorphism and stroke subtypes in Chinese.Journal of molecular neuroscience : MN · 2013Article
- Functional polymorphism of cyclooxygenase-2 gene (G-765C) in chronic obstructive pulmonary disease patients.Molecular biology reports · 2012Article
- TNF-alpha gene polymorphisms in Iranian Azari Turkish patients with inflammatory bowel diseases.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationArticle
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6 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCyclooxygenase-2 (COX-2) is a key enzyme involved in the conversion of arachidonic acid into prostaglandins. COX-2 is mainly induced at sites of inflammation in response to proinflammatory cytokines such as interleukin-1α/β, interferon-γ and tumor necrosis factor-α produced by inflammatory cells.
aimThe aim of this study was to investigate the possible modulating effect of the functional COX-2 polymorphisms -1195 A→G and -765G→C on the risk for development of inflammatory bowel disease (IBD) in a Dutch population.
methodsGenomic DNA of 525 patients with Crohn's disease (CD), 211 patients with ulcerative colitis (UC) and 973 healthy controls was genotyped for the -1195 A→G (rs689466) and -765G→C (rs20417) polymorphisms. Distribution of genotypes in patients and controls were compared and genotype-phenotype interactions were investigated.
resultsThe genotype distribution of the -1195A→G polymorphism was not different between the patients with CD or UC and the control group. The -765GG genotype was more prevalent in CD patients compared to controls with an OR of 1.33 (95%CI 1.04-1.69, p<0.05). The -765GC and -765CC genotype carriers showed a tendency to be less frequent in patients with CD compared to controls, with ORs of 0.78 (95%CI: 0.61-1.00) and 0.49 (95%CI 0.22-1.08), respectively. Combining homozygous and heterozygous patients with the -765C allele showed a reduced risk for developing CD, with an OR of 0.75 (95%CI: 0.59-0.96). In the context of this, the G(-1195)G(-765)/A(-1195)C(-765) diplotype was significantly less common in patients with CD compared to controls, with an OR of 0.62 (95%CI: 0.39-0.98). For UC however, such an effect was not observed. No correlation was found between COX-2 diplotypes and clinical characteristics of IBD.
conclusionsThe -765G→C polymorphism was associated with a reduced risk for developing Crohn's disease in a Dutch population.
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